Nocardia, an organism closely related to Mycobacterium, can cause fatal infections in man. Little is known about the mechanisms controlling nocardial invasion, infection, disease production and host immunity. In contrast, a great deal of work has been done on mycobacterial diseases. It has been shown that host immunity to mycobacteria is mainly a cell mediated type. Further, it has been shown with mycobacteria that much of the organism's effect on the host and host immunity as well as the organism's virulence resides in the chemical makeup of the cell envelope. Therefore, I propose to study the in vivo and in vitro chemical composition of nocardial cell walls. I shall explore the effect of the host as well as the environment on these components in order to determine how they effect the host-parasite relationship and host immunity. I shall compare and contrast the nocardial interactions with alveolar macrophages obtained from "Normal", "Immune", and "Compromised" rabbits. We shall investigate the effects of nocardial cell age, the effects of host-cell age (i.e., immature vs. mature host), the effects of specifically presensitized macrophages, the effects of specific immune sera, and the effects of certain Immunosuppressants on macrophage function in nocardial disease. At the same time I shall study the chemical composition of nocardial cell walls in vitro and in vivo in order to determine their specific role(s) in the host-parasite response. By using nocardia that vary from non-infectious to highly virulent forms, I should be able to establish more completely the factors contributing to nocardial virulence and the mechanisms that are involved in host-resistance and immunity.